There are two scenarios for the future course of BSE. The
first is that BSE, like TME and kuru, is a dead-end disease. If
this is true, and if meat and bone meal was the sole source of
the infection, then removing this source would be sufficient for
the eventual eradication of BSE from the United Kingdom.

In July 1988, the United Kingdom Government introduced a ban
on the feeding of all ruminant-derived protein to ruminants
(HMSO, 1988a; for subsequent modifications see HMSO, 1988e;
1989a; 1990b). However, the incubation period of BSE in cattle
averages about four to five years. This means that no reduction
in the current incidence can be expected until 1992 at the
earliest.

The alternative scenario is that there are natural routes of
transmission of BSE and that the outbreak could turn into an
endemic infection of cattle in the way that scrapie is in sheep.

As of July 1991 the ongoing epidemiological survey had not
revealed any firm evidence of maternal transmission of BSE, as
would be expected from the analogy with scrapie. Only one
putative case of maternal transmission in cattle has been
reported (Anon., 1991b).

A major experiment was set up in 1989 in order to investigate
this question. Carefully matched groups of test and control
animals are being observed to see if the incidence of BSE is
higher in calves born to BSE-affected dams. A high level of
maternal transmission of infection could be manifest after 1992.
A much longer observation period (up to a maximum of seven years)
will be necessary to prove a low incidence of maternal
transmission or to show that it does not occur.

To sustain BSE infection in the cattle population requires
that each breeding cow is replaced by at least one infected
female calf, which then transmits infection to at least one of
her offspring. The current breeding regimes in the United Kingdom
dairy herds, with an annual herd replacement rate of 20 to 25
percent, would not enable this to occur for a prolonged period of
time, even with a 100 percent maternal transmission of infection
to calves. Therefore, the worst that could happen in this
situation is that the rate of decline in the incidence of BSE
would be somewhat slower than if BSE were a dead-end infection
(Wilesmith and Wells, 1991).

For BSE to become endemic, the number of infected cattle would
need to increase by horizontal spread. In scrapie, this can occur
particularly at lambing as a by-product of the postnatal
component of maternal transmission. For example, an infected
placenta can be a source of infection to unrelated ewes.

Cattle management is sufficiently different from sheep
management for the chances of horizontal spread of BSE to be
lower, especially in dairy herds where cows often calve in
isolation and the calves are separated after a few days.

The same is not true of beef suckler herds in which cows and
calves run together. This would increase the chances of postnatal
maternal transmission and it might also create opportunities for
the horizontal spread of infection. However, BSE is much rarer in
beef than in dairy herds (see Table 4 and Wilesmith et al., 1988;
1992a).

In conclusion, BSE is unlikely to become an endemic infection
of cattle unless a high level of maternal transmission enables
the epidemic to be amplified by the horizontal spread of
infection. It is too soon to assess this possibility but it seems
improbable that BSE is highly contagious because the average
incidence within affected herds is only about 2 percent. There is
little point in imposing additional control measures until there
is a demonstrable need for them. However, common sense urges two
simple precautionary steps. The first is that calves born to cows
which are or which become confirmed cases of BSE should not be
selected as replacement heifers within the herd. The existence in
the United Kingdom of a specified offals ban means that such
calves could, for example, be fattened for beef without risk to
public health.

The second recommendation is to minimize the risk of
horizontal spread of infection at calving by good hygiene and the
early disposal of the placenta (by incineration or burial). This
is a legal requirement on those rare occasions when a suspect BSE
case is calving (HMSO, 1988b), but it is good practice for
reducing the spread of other infections as well.

Although unlikely, the worst possible situation would be if
BSE became established as an endemic infection in exactly the
same manner as scrapie. The difficulties of eradication would
then be similar.

Scrapie can be controlled quite effectively by selective
culling in the female line and by husbandry measures to limit the
horizontal spread of infection at lambing. But two problems make
this a difficult task.

The first is the need for accurate breeding records, which
rarely exist when most needed, at the start of the outbreak.
Selective culling cannot begin without them and it takes several
years to build up sufficient records.

The second problem is that infected ewe lines can only be
identified when the clinical disease appears. The spread of
infection from a ewe to several successive lamb crops can easily
go unnoticed for a generation if the anima dies or is culled
before developing the clinical disease. Since only a small
proportion of ewe lambs may be retained for breeding, another
infected generation could be missed if the few lambs that survive
as breeding ewes happen to be of a sip genotype which can be
infected but never develops the disease.

It therefore requires many years of patient application to
bring scrapie under control. Much of the work can easily be
undone if bought-in flock replacements reintroduce the infection.
This is why the eradication of scrapie is so difficult. The same
problems could attend the eradication of BSE, with one important
difference, described below.

In sheep, the sip gene has a major effect in controlling the
susceptibility and incubation period of scrapie. Sip and PrP
genes in sheep are almost certainly the same. The PrP gene is
also present in cattle and allelic variants have been found which
have either five or six copies of an octapeptide repeat sequence
in the coding region (Goldmann et al., 1991).

However, studies of a large herd affected with multiple cases
showed no association of BSE with this polymorphism of the PrP
gene (Dawson and Martin, personal communication). These findings
are consistent with the biological evidence (particularly from
transmission studies as mentioned in Chapter 4, suggesting that
there may be little or no allelic variation at the PrP or any
other genetic locus that affects BSE. If true, the occurrence of
infected carriers may be far less common in BSE than in scrapie,
making BSE easier to eradicate.

If further steps to eradicate BSE become necessary, they would
not be worth applying on less than a national scale. The
essential prerequisite is good breeding and movement records
which are currently being compiled in the United Kingdom
following recent legislation (HMSO, 1990c; 1990d). By the time
they are sufficient for the task, the necessity (or otherwise)
for further action to eradicate BSE will be known. Meanwhile, the
precautionary measures to safeguard other species, including
human beings, are already in place.